大豆斑疹病菌铁摄取因子PiuB在致病性中的作用分析

The role of iron-uptake factor PiuB in pathogenicity of soybean pathogen Xanthomonas axonopodis pv.glycines

铁作为生命必需的基本元素,在细菌生长代谢过程中具有重要作用。然而,大豆斑疹病菌(Xanthomonas axonopodis pv.glycines,Xag)中编码铁摄取因子的piuB基因是否参与病原菌的铁摄取和致病性并不清楚。为解析PiuB的作用,采用同源重组策略获得了Xag的piuB基因缺失突变株(ΔpiuB),并对该突变株进行功能研究。研究表明:相较于野生型,突变株ΔpiuB在寄主大豆上的毒性和生长能力显著削弱;铁载体分泌量激增;对Fe^(3+)、Cu^(2+)、Zn^(2+)和Mn^(2+)的敏感性显著增强。此外,该突变株的H_(2)O_(2)抗性、胞外多糖产量、生物膜形成能力以及游动性等相较于野生型均显著减弱;添加外源Fe^(3+)不能有效恢复ΔpiuB的上述特性;功能互补株可完全恢复ΔpiuB的缺陷性表型至野生型水平。这说明PiuB是Xag摄取Fe^(3+)的潜在因子,并且是Xag在寄主大豆上致病所需的。

Iron is an essential element for living organisms that plays critical roles in the process of bacterial growth and metabolism.However,it remains to be elucidated whether piuB encoding iron-uptake factor is involved in iron uptake and pathogenicity of Xanthomonas axonopodis pv.glycines(Xag).To investigate the function of piuB,we firstly generated a piuB deletion mutant(ΔpiuB)by homologous recombination.Compared with the wild-type,the piuB mutant exhibited significantly reduced growth and virulence in host soybean.The mutant displayed markedly increased siderophore secretory volume,and its sensitivity to Fe^(3+),Cu^(2+),Zn^(2+)and Mn^(2+)was significantly enhanced.Additionally,the H_(2)O_(2) resistance,exopolysaccharide yield,biofilm formation,and cell mobility ofΔpiuB were significantly diminished compared to that of the wild-type.The addition of exogenous Fe^(3+)cannot effectively restore the above characteristics of ΔpiuB.However,expressing piuB in trans rescued the properties lost by ΔpiuB to the levels in the wild-type.Taken together,our results demonstrated that PiuB is a potential factor for Xag to assimilate Fe^(3+),and is necessary for Xag to be pathogenic in host soybean.